Document Detail


Hyperoxia alters the mechanical properties of alveolar epithelial cells.
MedLine Citation:
PMID:  22467640     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Patients with severe acute lung injury are frequently administered high concentrations of oxygen (>50%) during mechanical ventilation. Long-term exposure to high levels of oxygen can cause lung injury in the absence of mechanical ventilation, but the combination of the two accelerates and increases injury. Hyperoxia causes injury to cells through the generation of excessive reactive oxygen species. However, the precise mechanisms that lead to epithelial injury and the reasons for increased injury caused by mechanical ventilation are not well understood. We hypothesized that alveolar epithelial cells (AECs) may be more susceptible to injury caused by mechanical ventilation if hyperoxia alters the mechanical properties of the cells causing them to resist deformation. To test this hypothesis, we used atomic force microscopy in the indentation mode to measure the mechanical properties of cultured AECs. Exposure of AECs to hyperoxia for 24 to 48 h caused a significant increase in the elastic modulus (a measure of resistance to deformation) of both primary rat type II AECs and a cell line of mouse AECs (MLE-12). Hyperoxia also caused remodeling of both actin and microtubules. The increase in elastic modulus was blocked by treatment with cytochalasin D. Using finite element analysis, we showed that the increase in elastic modulus can lead to increased stress near the cell perimeter in the presence of stretch. We then demonstrated that cyclic stretch of hyperoxia-treated cells caused significant cell detachment. Our results suggest that exposure to hyperoxia causes structural remodeling of AECs that leads to decreased cell deformability.
Authors:
Esra Roan; Kristina Wilhelm; Alex Bada; Patrudu S Makena; Vijay K Gorantla; Scott E Sinclair; Christopher M Waters
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-03-30
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  302     ISSN:  1522-1504     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-06-18     Completed Date:  2012-08-23     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L1235-41     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Actins / metabolism
Animals
Cell Adhesion
Cell Line
Cell Shape
Cells, Cultured
Cytochalasin D / pharmacology
Elastic Modulus / drug effects
Finite Element Analysis
Hyperoxia / pathology*,  physiopathology*
Male
Mechanotransduction, Cellular
Mice
Microscopy, Atomic Force
Microtubules / metabolism,  ultrastructure
Oxygen
Pneumocytes / pathology*,  physiology*
Rats
Rats, Sprague-Dawley
Reactive Oxygen Species / metabolism
Respiration, Artificial / adverse effects
Signal Transduction
Stress, Physiological
Grant Support
ID/Acronym/Agency:
HL094366/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Actins; 0/Reactive Oxygen Species; 22144-77-0/Cytochalasin D; 7782-44-7/Oxygen
Comments/Corrections
Comment In:
Am J Physiol Lung Cell Mol Physiol. 2012 Jun 15;302(12):L1233-4   [PMID:  22523279 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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